CAJ | 학술논문

目的研究N-(4-羟基苯基)维生素甲酰胺(4-HPR)对人肺腺癌细胞A549体外迁移能力的影响及其作用机制。方法1μmol/L 全反式维甲酸( ATRA)和4-HPR处理肺腺癌A549细胞24 h后，细胞划痕实验检测其对A549细胞体外迁移能力的影响；Western blot法检测骨桥蛋白( OPN)、肌球蛋白轻链激酶( MLCK)的表达和肌球蛋白轻链( MLC)磷酸化程度；细胞划痕实验观察 MLCK抑制剂 ML-7对 A549细胞迁移能力的影响。结果1μmol/L 4-HPR处理的A549细胞与细胞对照以及溶剂对照细胞相比，迁移距离明显降低(P<0.05)；Western blot分析结果表明1μmol/L 4-HPR可明显降低 A549细胞 MLCK 的表达和 MLC 磷酸化( P <0.05)，而对OPN表达无显著影响；ML-7可明显减少 A549细胞迁移距离( P <0.05)。结论4-HPR 可能通过减少MLCK的表达和MLC磷酸化，抑制A549细胞的体外迁移。
목적연구N-(4-간기분기)유생소갑선알(4-HPR)대인폐선암세포A549체외천이능력적영향급기작용궤제。방법1μmol/L 전반식유갑산( ATRA)화4-HPR처리폐선암A549세포24 h후，세포화흔실험검측기대A549세포체외천이능력적영향；Western blot법검측골교단백( OPN)、기구단백경련격매( MLCK)적표체화기구단백경련( MLC)린산화정도；세포화흔실험관찰 MLCK억제제 ML-7대 A549세포천이능력적영향。결과1μmol/L 4-HPR처리적A549세포여세포대조이급용제대조세포상비，천이거리명현강저(P<0.05)；Western blot분석결과표명1μmol/L 4-HPR가명현강저 A549세포 MLCK 적표체화 MLC 린산화( P <0.05)，이대OPN표체무현저영향；ML-7가명현감소 A549세포천이거리( P <0.05)。결론4-HPR 가능통과감소MLCK적표체화MLC린산화，억제A549세포적체외천이。
Objective To investigate the influences of N-(4-hydroxyphenyl) retinoide (4-HPR) on the migration of human lung adenocarcinoma cells and its mechanism. Methods Cell scarification test was performed to measure the migration of A549 cells treated with 1μmol/L 4-HPR. The expression level of osteopontin( OPN) , myosin light chain kinase( MLCK) and phosphorylation of myosin light chain( MLC) in A549 cells treated by 4-HPR was detec-ted by Western blot, respectively. The effect of ML-7, a selective inhibitor of MLCK, on the migration of A549 cells was analyzed by cell scarification test. Results Compared with cell and solvent control group, the migration distance of A549 cells treated with 1 μmol/L 4-HPR was obviously decreased(P<0.05). The Western blot analy-sis showed that 1 μmol/L 4-HPR could significantly reduce the expression of MLCK and phosphorylation of MLC protein (P<0.05), while had no influence on the expression of OPN. ML-7 could decrease the distances of migra-tion of A549 cells notably ( P<0.05 ) . Conclusion 4-HPR may inhibit the migration of A549 cells through de-creasing the expression of MLCK and phosphorylation of MLC protein.